happen high positive anti histone antibody What causes anti anti-histone antibodies positive

What can happen with a high positive anti histone antibody

Antibody Assays

Test for the presence of antinuclear antibodies, which can appear in a homogeneous pattern in as many as 90% of patients with lupus erythematosus. In drug-induced lupus erythematosus (DILE), when anti-ssDNA and anti-dsDNA are measured, the prevalence of anti-ssDNA is higher. This is a major difference from systemic lupus erythematosus (SLE); in SLE, antibodies tend to attack double-stranded DNA.

Antinuclear antibodies with homogeneous patterns are produced by procainamide, isoniazid, timolol, hydralazine, and phenytoin. In contrast, speckled antinuclear antibody patterns are associated with anti-SSA/Ro antibodies, which can be produced in response to thiazide diuretics such as hydrochlorothiazide. A systematic review evidenced that anti-SSA/Ro antibodies are found in most patient with DISCLE (about 80% of cases), in whom antihistone antibodies are uncommonly found, and most remained positive after resolution of SCLE skin disease activity. [7]

In persons with DILE, the antibodies also tend to attack histones (proteins typically found in cell nuclei). Antihistone antibodies are indicated by a homogeneous pattern of antinuclear antibodies. They are present in more than 75% of patients with DILE induced by hydralazine and procainamide. An example of an antihistone antibody that is often implicated in DILE is immunoglobulin G (IgG; anti-[H2A-H2B] DNA). Antihistone antibodies are much more likely to indicate DILE; however, they can also appear in as many as 50% of patients with SLE.

In persons with DILE, anti-Sm antibodies are rare. Complement levels are within the reference range, which is not usually the case in persons with SLE.

Other Tests

Further tests in the workup of a patient with possible DILE are as follows.

A complete blood count (CBC) should be performed to evaluate for anemia, which is present in most patients with SLE but is rare in those with DILE. Blood urea nitrogen (BUN) and creatinine should be assessed. C3 and C4 levels should be measured. Complement levels are often reduced in persons with SLE, whereas they tend to not be reduced in persons with DILE.

Liver function tests to can be performed to evaluate for hepatic involvement. Urinalysis can be performed to evaluate for hematuria and proteinuria.

Use chest radiography to rule out pulmonary infiltrates. Use echocardiography, if indicated, to rule out pericarditis.

Tissue Analysis and Histologic Findings

Skin biopsy may be indicated, as well as renal biopsy if renal involvement is suggested. Skin biopsy and direct immunofluorescence typically reveal findings that are indistinguishable from those seen in SLE.

Histologic examination reveals variable epidermal atrophy, basal vacuolar degeneration, apoptotic or dyskeratotic keratinocytes, and lymphocytic interface dermatitis (see the images below).

Dermis contains interface and superficial and deep perivascular lymphohistiocytic infiltrate (×100, hematoxylin-eosin).

Parakeratosis, apoptosis, and basal vacuolization (×200, hematoxylin-eosin).

Direct immunofluorescence may reveal granular deposition of IgG along the dermoepidermal junction.

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Author

Coauthor(s)

Eli Hernandez, BS Trainee/Student, Georgetown Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Ivan D Camacho, MD Dermatologist, Private Practice; Voluntary Assistant Professor of Dermatology, Department of Dermatology and Cutaneous Surgery, University of Miami, Leonard M Miller School of Medicine

Ivan D Camacho, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Florida Medical Association, International Society of Dermatology, Women's Dermatologic Society

Disclosure: Nothing to disclose.

Caroline O Amin, MD Resident Physician, Department of Pediatrics, Connecticut Childrens Medical Center, University of Connecticut School of Medicine

Caroline O Amin, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Consulting fee Consulting; Celgene Honoraria Safety Monitoring Committee; GSK - Glaxo Smith Kline Consulting fee Consulting; TenXBioPharma Consulting fee Safety Monitoring Committee

Craig A Elmets, MD Professor and Chair, Department of Dermatology, Director, UAB Skin Diseases Research Center, University of Alabama at Birmingham School of Medicine

Craig A Elmets, MD is a member of the following medical societies: American Academy of Dermatology, American Association of Immunologists, American College of Physicians, American Federation for Medical Research, and Society for Investigative Dermatology

Disclosure: Palomar Medical Technologies Stock None; Astellas Consulting fee Review panel membership; Massachusetts Medical Society Salary Employment; Abbott Laboratories Grant/research funds Independent contractor; UpToDate Salary Employment; Biogen Grant/research funds Independent contractor; Clinuvel Independent contractor; Covan Basilea Pharmaceutical Grant/research funds Independent contractor; ISDIN None Consulting; TenX BIopharma Grant/research funds Independent contractor

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

What causes anti

AHA are frequently produced by patients suffering from systemic lupus erythematosus and drug-induced lupus, and also from other autoimmune, neurological and infectious diseases.

What causes high histone levels?

Levels of circulating histones as well as nucleosomes are increased in animals or patients with cancer, inflammation, and infection, suggesting an extracellular role of histones in human disease. Histone is released from activated immune cells (e.g., neutrophils23 and mast cells24) by extracellular traps.

Which tests would be positive for histones?

Anti-histone antibodies can be clinically detected using an ELISA assay. A blood sample is required for the test.

How do you test for drug

A laboratory test called the antinuclear antibody panel (ANA) is used to check your blood for histone-DNA complex antibodies. The presence of these antibodies suggests a diagnosis of drug-induced lupus. Some people who have lupus due to quinidine or hydralazine may test ANA-negative.

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